The aims of this grant are (1 to place mutations affecting the retina in mice onto a few selected genetic backgrounds by standard breeding schedules, so that the gene actions can be more accurately compared and contrasted with one another, 2) to distribute affected and control mice or tissues or chemical extracts to qualified research scientists at no charge to them except for shipping costs, so that they can carry on their research without committing the time or bearing the expense of generating their own mice, and 3) to mutagenize male mice and mate them with females carrying known retinal mutations, so as to select for new mutant alleles that will illuminate how particular genes control retinal function and cause disease. Progeny of mutagenized mice will be screened for retinal disease by nondestructive indirect ophthalmoscopy, a rapid and effective method that markedly reduces the need to screen laboriously by expensive histological methods.These mouse models have been adding significantly to our understanding of inherited diseases of the retinitis pigmentosa category in humans, and are likely to contribute even more crucially in the years immediately ahead. The most widely used mutations at present are named retinal degeneration (rd), retinal degeneration slow (rds), Purkinje cell degeneration (pcd), and nervous (nr). We maintain each of these on several genetic backgrounds, including three independently-occurring mutant alleles at the pcd locus. We have developed, or are developing, most of these strains, and are the unique holder of several of them. Additionally, we will supply mice with new retinal disorders named hugger (hug), vitiligo (vit), and wabbler lethal-2J (wl2J); these affect not only retinal photoreceptor cells, the hallmark of the retinitis pigmentosa class of diseases, but also affect other components of the retina, and thus open the prospect of deepening our understanding of genetic control and functions of cells in retinal pigment epithelium and inner nuclear and ganglion cell layers. Further available mutants serve as models of congenital stationary night blindness. Still others cause hypopigmentation and developmental abnormalities in the trajectories of ganglion cell axons in the optic nerve. We are prepared also to advise other investigators, as we have done during the first funding cycle of this grant, concerning what mutants, genetic backgrounds, controls, ages, and numbers of mice might help to solve their research questions. Another service function will be to take on the propagation and dissemination of mutant stocks, including transgenic mice with retinal abnormalities, that are developed by other investigators who may not wish to remain solely responsible for holding and distributing such research material.